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ATP released from beta-amyloid-stimulated microglia induces reactive oxygen species production in an autocrine fashion.

Authors
Kim, SY; Moon, JH; Lee, HG; Kim, SU; Lee, YB
Citation
Experimental & molecular medicine, 39(6):820-827, 2007
Journal Title
Experimental & molecular medicine
ISSN
1226-36132092-6413
Abstract
Present study demonstrated that fibrillar beta-amyloid peptide (fAbeta1-42) induced ATP release, which in turn activated NADPH oxidase via the P2X7 receptor (P2X7R). Reactive oxygen species (ROS) production in fAbeta1-42- treated microglia appeared to require Ca2+ influx from extracellular sources, because ROS generation was abolished to control levels in the absence of extracellular Ca2+. Considering previous observation of superoxide generation by Ca2+ influx through P2X7R in microglia, we hypothesized that ROS production in fAbeta-stimulated microglia might be mediated by ATP released from the microglia. We therefore examined whether fAbeta1-42-induced Ca2+ influx was mediated through P2X7R activation. In serial experiments, we found that microglial pretreatment with the P2X7R antagonists Pyridoxal-phosphate-6-azophenyl-2',4'- disulfonate (100 microM) or oxidized ATP (100 microM) inhibited fAbeta-induced Ca2+ influx and reduced ROS generation to basal levels. Furthermore, ATP efflux from fAbeta1-42- stimulated microglia was observed, and apyrase treatment decreased the generation of ROS. These findings provide conclusive evidence that fAbeta-stimulated ROS generation in microglial cells is regulated by ATP released from the microglia in an autocrine manner.
MeSH terms
Adenosine Triphosphate/metabolism*Amyloid beta-Peptides/pharmacology*AnimalsAutocrine Communication/drug effects*Autocrine Communication/physiologyCells, CulturedMicroglia/drug effects*Peptide Fragments/pharmacology*Pyridoxal Phosphate/analogs & derivativesPyridoxal Phosphate/metabolismRatsRats, Sprague-DawleyReactive Oxygen Species/metabolism*Receptors, Purinergic P2/physiology
DOI
10.1038/emm.2007.89
PMID
18160853
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
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